论文部分内容阅读
目的观察STAT1信号分子和T-bet转录因子在咪喹莫特诱导的银屑病疾病模型中的不同作用。方法将雄性8周龄129和C57BL/6小鼠分别随机分为正常对照组、野生型咪喹莫特诱导组,将雄性8周龄STAT1-/-小鼠和T-bet-/-小鼠分为STAT1-/-咪喹莫特诱导组、T-bet-/-咪喹莫特诱导组,依据PASI评分标准记录评价小鼠银屑病疾病模型的严重程度,HE染色观察疾病模型中皮损组织的形态和炎性细胞浸润情况来评价其病理学改变,实时荧光定量PCR检测疾病模型的皮损组织中相关细胞因子基因表达水平的改变。结果局部给予咪喹莫特诱导后4种小鼠(129、C57BL/6、STAT1-/-、T-bet-/-)背部皮肤均出现不同程度红斑、鳞屑、炎症细胞浸润。与T-bet-/-对比,STAT1-/-给药组皮炎反应更严重。与野生型给药组相比,STAT1-/-给药组分泌的IL-22水平明显升高而IL-17升高不明显。结论 STAT1信号分子可能通过除Th17细胞分泌外的其他途径调控IL-22表达水平,从而影响银屑病严重程度。
Objective To observe the different roles of STAT1 signaling molecule and T-bet transcription factor in imiquimod-induced psoriasis disease model. Methods Eighty male Wistar rats aged 8 weeks and C57BL / 6 mice were randomly divided into normal control group, wild type imiquimod induction group, male 8 weeks old STAT1 - / - mice and T-bet - / - mice The mice were divided into STAT1 - / - imiquimod - induced group and T - bet - / - imiquimod - induced group. The severity of the mouse psoriasis model was evaluated according to PASI score standard. The pathological changes were evaluated by morphological changes and inflammatory cell infiltration. Real-time quantitative PCR was used to detect the expression of related cytokine genes in the lesion tissues. RESULTS: Inflammatory cells and infiltration of erythematous, scaly and inflammatory cells were found in the back of 4 mice (129, C57BL / 6, STAT1 - / -, T-bet - / -) treated with imiquimod locally. Compared with T-bet - / -, dermatitis was more severe in STAT1 - / - administration group. Compared with the wild-type group, the level of IL-22 secreted by STAT1 - / - administration group was significantly increased while the increase of IL-17 was not obvious. Conclusion STAT1 signaling molecules may regulate the expression of IL-22 through other ways than the secretion of Th17 cells, thereby affecting the severity of psoriasis.